Bodey B, Bodey B, Siegel S E, Kaiser H E
Department of Pathology, School of Medicine, University of Southern California, Los Angeles, USA.
In Vivo. 1998 Jan-Feb;12(1):107-22.
In mammalian cells, neoplastic transformation is directly associated with the expression of oncogenes, with the mutation, loss or simple inactivation of the function of tumor suppressor genes, and the production of certain growth factors. Genes for suppression of the development of the malignant immunophenotype, as well as inhibitory growth factors have regulatory functions within the normal processes of cell division and differentiation. Telomerase (a ribonucleoprotein polymerase) activation is frequently observed in various cancers. Telomerase activation is regarded as essential for cell immortalization and its inhibition may result in the spontaneous regression (SR) of neoplasms. SR of neoplasms occurs when the malignant tumor mass partially or completely disappears without any treatment or as a result of a therapy considered inadequate to influence systemic neoplastic disease. This definition makes it clear that the term SR applies to neoplasms in which the malignant disease is not necessarily cured, and to cases where the regression may be neither complete nor permanent. A number of possible mechanisms of SR are reviewed, with the understanding that no single mechanism can completely account for this phenomenon. The application of the newest immunological, molecular biological and genetic insights for more individualized anticancer immunotherapy (biotherapy) is also discussed.
在哺乳动物细胞中，肿瘤转化与癌基因的表达、肿瘤抑制基因功能的突变、缺失或简单失活以及某些生长因子的产生直接相关。抑制恶性免疫表型发展的基因以及抑制性生长因子在细胞分裂和分化的正常过程中具有调节功能。端粒酶（一种核糖核蛋白聚合酶）激活在各种癌症中经常被观察到。端粒酶激活被认为是细胞永生化所必需的，其抑制可能导致肿瘤的自发消退（SR）。当恶性肿瘤块在没有任何治疗的情况下部分或完全消失，或者由于被认为不足以影响全身性肿瘤疾病的治疗而消失时，就会发生肿瘤的SR。这个定义明确表明，SR这个术语适用于恶性疾病不一定被治愈的肿瘤，以及消退可能既不完全也不持久的情况。本文综述了SR的一些可能机制，但要明白没有单一机制能完全解释这一现象。还讨论了最新的免疫学、分子生物学和遗传学见解在更个体化的抗癌免疫治疗（生物治疗）中的应用。
